The present research has demonstrated that environmental stressors, acting during prenatal but not postnatal periods of sexual differentiation, feminize and demasculinize the sexual behavior of male rats. Prolonged treatment of prenatally stressed males in adulthood with the male hormone testosterone propionate, results in some increases in male copulatory behavior, but this is accompanied by an increase in female behavior not found in similarly treated normal males. The sexual behavior of pre- and/or postnatally stressed females was not altered. It has been repeatedly demonstrated that these types of behavioral modifications in males are brought about by a reduced output of endogenous testiclar androgen. The mechanism postulated as mediating the prenatal stress syndrome seen in our animals is stress induced hyposecretion of the primary gonadal androgen, testosterone during critical prenatal stages of sexual behavior differentiation. A series of experiments are in progress or are proposed to delineate the limits of such alterations in sexual behavior potentials and to identify the mechanisms mediating them.